Scientists believe amyloid protein plays a role in Alzheimer’s but are still trying to explain how.

One of the hallmarks of Alzheimer’s disease, which is characterized by memory loss and dementia, is a protein called amyloid. In patients who die of the disease, sticky plaques of the protein are found in the brain at autopsy, although not all people with amyloid deposits develop Alzheimer’s. But why does the protein start to gum up the delicate network of nerves in the brain? Some recent evidence suggested that the protein, which the body makes normally in small amounts, spreads from one cell to another in the brain of affected patients, eventually compromising multiple regions of the brain over time.

But a new study published in the journal JAMA Neurology found no evidence to suggest such a contagion-based model for the disease, nor did it find that Alzheimer’s proteins can be transmitted from one person to another.

Some previous work suggested that amyloid might act as a prion, or proteins that have the unique ability to fold in abnormal ways and then pass from cell to cell. In diseases such as bovine spongiform encephalopathy, or mad cow in animals, and in Creutzfeldt-Jakob disease in people, prions also pass from host to host. Prions can spread from contaminated food, or through blood transfusion of blood or tissue transplants from infected individuals.

To determine whether similar prions were at work in neurodegenerative diseases such as Alzheimer’s or Parkinson’s, researchers studied people who had received human growth hormone from 1963 to 1985 derived from cadavers. In the mid-1980s, over 200 of these patients developed Creutzfeldt-Jakob disease after being inadvertently infected with prion proteins from affected donor tissue. Since then, this group of patients has been closely monitored with extensive medical records to track for further cases.

The researchers looked for signs of an elevated risk of Alzheimer’s, Parkinson’s, frontotemporal lobar degeneration and amyotrophic lateral sclerosis (ALS) among the recipients. They found small amounts of amyloid protein in some growth hormone patients, and three cases of ALS, but no cases of Alzheimer’s or Parkinson’s.

“People wonder if it will be possible for a person with Alzheimer’s disease to infect another individual without Alzheimer’s disease, if a kidney transplant came from an Alzheimer’s patient,” says the study’s senior author, Dr. John Trojanowski of the Center for Neurodegenerative Disease Research and the Institute on Aging at the University of Pennsylvania School of Medicine. “It’s still something one can debate of course, but our findings argue there is no evidence in this large cohort of human-to-human transmission. The likelihood of a transplant conveying the disease would be very low.”

And while amyloid may not be “contagious,” other research confirms the role it plays in the development of the disease. In a separate study, published in the Proceedings of the National Academy of Sciences, researchers from Weill Cornell Medical College studied mice that were genetically modified to develop amyloid in their brains and blood vessels. Then, to see if lowering amyloid burden can reduce signs of Alzheimer’s, the researchers removed a receptor called CD36 that appears on the surface of immune cells and is linked to amyloid buildup.

They found that mice without CD36 had less amyloid in their brain vessels and performed better on cognitive tests, which suggests that removing protein from arteries can reduce symptoms of the disease. The results also hint that reducing levels of CD36 might be an effective way to slow the cognitive decline of Alzheimer’s.

“Our findings strongly suggest that amyloid, in addition to damaging neurons, also threatens the cerebral blood supply and increases the brain’s susceptibility to damage through oxygen deprivation,” says the study’s senior investigator, Dr. Costantino Iadecola, a professor of neurology at Weill Cornell Medical College and director of the Brain and Mind Research Institute at Weill Cornell Medical College and New York—Presbyterian Hospital. “If we can stop accumulation of amyloid in these blood vessels, we might be able to significantly improve cognitive function in Alzheimer’s-disease patients. Furthermore, we might be able to improve the effectiveness of amyloid immunotherapy, which is in clinical trials but has been hampered by the accumulation of amyloid in cerebral blood vessels.”

Taken together, the two studies provide important insight into how Alzheimer’s works to affect memory and other cognitive functions, and may lead to more effective ways to slow, if not necessarily inhibit, the progressive decline that makes the disease so challenging to treat.

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